Removal of one kidney results in a prompt increase in electrolyte excretion by the remaining kidney. This increase occurs without change in glomerular filtration rate, hematocrit, or plasma protein concentration, and despite a fall in renal blood flow. Acute unilateral nephrectomy also causes a consistent fall in cardiac output and a rise in total peripheral resistance; mean arterial pressure does not increase significantly, but diastolic pressure rises, and heart rate falls. When these hemodynamic changes are prevented, the natriuresis by the remaining kidney does not occur, suggesting that the alterations in systemic hemodynamics are an important aspect of the functional response of the remaining kidney to acute uninephrectomy. The objectives of the proposed research are to characterize more fully the consequences of acute uninephrectomy by studying the possible afferent and efferent limbs of a neurocirculatory reflex arc initiated by nephrectomy. The renal response will be evaluated in studies designed to localize the nephron segment chiefly responsible for the decrease in sodium reabsorption. Since the hemodynamic changes following uninephrectomy resemble those seen on closure of a chronic arteriovenous fistula, dogs wih surgically constructed A-V fistulae will be studied to determine if the renal response to fistula closure matches the response to uninephrectomy. Finally, the importance of these hemodynamic alterations to the onset of compensatory renal hypertrophy will be assessed. These studies will extend knowledge of the relationship of circulatory adjustements to regulation of sodium balance, and in addition provide valuable insights into the mechanisms of compensatory renal hypertrophy.